ArticlePloS one2013
The severity of experimental autoimmune cystitis can be ameliorated by anti-CXCL10 Ab treatment.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Animal Models of Hunner-Type Interstitial Cystitis.International journal of urology : official journal of the Japanese Urological Association · 2026Review
- Inhibition of microRNA-34c reduces detrusor ROCK2 expression and urinary bladder inflammation in experimental cystitis.Life sciences · 2024Article
- Animal models of interstitial cystitis/bladder pain syndrome.Frontiers in physiology · 2023Review
- Therapeutic potential of nanoceria pretreatment in preventing the development of urological chronic pelvic pain syndrome: Immunomodulation via reactive oxygen species scavenging and SerpinB2 downregulation.Bioengineering & translational medicine · 2023Article
- Broaden Horizons: The Advancement of Interstitial Cystitis/Bladder Pain Syndrome.International journal of molecular sciences · 2022Review
- Roles of mesenchymal stem cells and exosomes in interstitial cystitis/bladder pain syndrome.Journal of cellular and molecular medicine · 2022Review
- TRPV4 activation prevents lipopolysaccharide-induced painful bladder hypersensitivity in rats by regulating immune pathways.Frontiers in immunology · 2022Article
- The NLRP3 Inflammasome Inhibitor Dapansutrile Attenuates Cyclophosphamide-Induced Interstitial Cystitis.Frontiers in immunology · 2022Article
- Circulatory Inflammatory Mediators in the Prediction of Anti-Tuberculous Drug-Induced Liver Injury Using RUCAM for Causality Assessment.Biomedicines · 2021Article
- Differential Expression of microRNAs Correlates With the Severity of Experimental Autoimmune Cystitis.Frontiers in immunology · 2021Article
- Interstitial cystitis/bladder pain syndrome: The evolving landscape, animal models and future perspectives.International journal of urology : official journal of the Japanese Urological Association · 2020Review
- The combination of CXCL9, CXCL10 and CXCL11 levels during primary HIV infection predicts HIV disease progression.Journal of translational medicine · 2019Article
- Expression and Function of Chemokines CXCL9-11 in Micturition Pathways in Cyclophosphamide (CYP)-Induced Cystitis and Somatic Sensitivity in Mice.Frontiers in systems neuroscience · 2018Article
- Serum Cytokine Profiling in Cats with Acute Idiopathic Cystitis.Journal of veterinary internal medicine · 2018Article
- CXCL10/IP-10 Neutralization Can Ameliorate Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome in Rats.PloS one · 2017Article
- Increased CXCR3 Expression of Infiltrating Plasma Cells in Hunner Type Interstitial Cystitis.Scientific reports · 2016Article
- Stem Cell Therapy for Interstitial Cystitis/Bladder Pain Syndrome.Current urology reports · 2016Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
backgroundInterstitial cystitis (IC), more recently called painful bladder syndrome (PBS) is a complex disease associated with chronic bladder inflammation that primarily affects women. Its symptoms include frequent urinary urgency accompanied by discomfort or pain in the bladder and lower abdomen. In the United States, eight million people, mostly women, have IC/PBS. New evidence that autoimmune mechanisms are important in the pathogenesis of IC/PBS triggered interest. METHODOLOGY/PRINCIPAL
findingsSWXJ mice immunized with a homogenate of similar mice's urinary bladders develop an autoimmune phenotype comparable to clinical IC with functional and histological alterations confined to the urinary bladder. Using the murine model of experimental autoimmune cystitis (EAC), we found that serum levels of CXCR3 ligand and local T helper type 1 (Th1) cytokine are elevated. Also, IFN-γ-inducible protein10 (CXCL10) blockade attenuated overall cystitis severity scores; reversed the development of IC; decreased local production of CXCR3 and its ligands, IFN-γ, and tumor necrosis factor-α (TNF-α); and lowered systemic levels of CXCR3 ligands. Urinary bladder CD4(+) T cells, mast cells, and neutrophils infiltrates were reduced following anti-CXCL10 antibody (Ab) treatment of mice. Anti-CXCL10 Ab treatment also reversed the upregulated level of CXCR3 ligand mRNA at urinary bladder sites. The decreased number and percentage of systemic CD4(+) T cells in EAC mice returned to normal after anti-CXCL10 Ab treatment. CONCLUSION/SIGNIFICANCE: Taken together, our findings provide important new information about the mechanisms underlying EAC pathogenesis, which has symptoms similar to those of IC/PBS. CXCL10 has the potential for use in developing new therapy for IC/PBS.
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